This review presents evidence for the immunopathogenesis of psoriasis. T lymphocytes with human lymphocyte antigen (HLA)-DR molecules and receptors for interleukin 2 were found in the dermis of psoriatic plaques, suggesting the presence of activated T cells in these lesions. Keratinocytes in active plaques demonstrated HLA-DR molecules on their surfaces. These immunologic abnormalities were reversible with medical therapy. Keratinocyte HLA-DR expression was associated with an increased incidence of psoriatic arthritis. We propose that HLA-DR + keratinocytes and Langerhans cells in plaques could activate dermal T cells directly in an autologous mixed leucocyte/epithelial cell reaction. Alternatively, they could present an unknown autologous or exogenous antigen to T lymphocytes. T cell activation would then lead to the release of mediators of inflammation, and possibly of epidermal growth factors. This hypothesis also provides an explanation for the chronicity of psoriasis. Most of the therapies used to treat psoriasis suppress cellular immune function and inflammation. These include ultraviolet irradiation, cyclosporine, corticosteroids, methotrexate, anthralin, and retinoids.